ライフサイエンスコーパス: Cl- channel

1 increases intraluminal liquidity by opening Cl channels.

2 nates in opening of a ciliary Ca2+-activated Cl- channel.

3 es, mediated by Kv1.3 and outward rectifying Cl- channels.

4 SLC26A7 and SLC26A9 function exclusively as Cl- channels.

5 iate the effects of presynaptic ligand-gated Cl- channels.

6 calcium-activated K+ channels, Na+,Ca2+, and Cl- channels.

7 and a subsequent opening of plasma membrane Cl- channels.

8 ceptors by transport mechanisms that utilize Cl- channels.

9 ) and pharmacologic inhibitors of epithelial Cl - channels.

10 ecting duct cells, claudin-4 functioned as a Cl(-) channel.

11 ICC express ANO1, a Ca(2+)-activated Cl(-) channel.

12 ithelium in which it probably functions as a Cl(-) channel.

13 fibrosis transmembrane conductance regulator Cl(-) channel.

14 al properties similar to the mammalian ClC-2 Cl(-) channel.

15 opens during the transport cycle to form the Cl(-) channel.

16 nductance regulator (CFTR), a cAMP-regulated Cl(-) channel.

17 chloride ion (Cl(-)) efflux through the CFTR Cl(-) channel.

18 nsmembrane glycoprotein and a cAMP-activated Cl(-) channel.

19 s transmembrane conductance regulator (CFTR) Cl(-) channel.

20 s for eukaryotic Cl(-)/H(+) transporters and Cl(-) channels.

21 multiple cell types but did not affect CFTR Cl(-) channels.

22 defect mediated by the molecularly distinct Cl(-) channels.

23 consists of both Cl(-)/H(+) antiporters and Cl(-) channels.

24 is accomplished by Cl(-) efflux through ClC3 Cl(-) channels.

25 a(2+) channels in addition to functioning as Cl(-) channels.

26 s transmembrane conductance regulator (CFTR) Cl(-) channels.

27 macular dystrophy via dysfunction of hBest1 Cl(-) channels.

28 ayed deactivation of individual F508del-CFTR Cl(-) channels.

29 s transmembrane conductance regulator (CFTR) Cl(-) channels.

30 Bestrophins are a newly identified family of Cl(-) channels.

31 fibrosis transmembrane conductance regulator Cl(-) channels.

32 s activation of alternative Ca(2+)-dependent Cl(-) channels.

33 )-channels and, indirectly, Ca(2+)-activated Cl(-) channels.

34 vely, confirming that STICs were mediated by Cl(-) channels.

35 d Ca(2+) signal to activate Ca(2+)-dependent Cl(-) channels.

36 st that curcumin may directly stimulate CFTR Cl(-) channels.

37 hrinkage by opening TMEM16A Ca(2+)-activated Cl(-) channels.

38 hibition of the cell surface density of CFTR Cl(-) channels.

39 function as both amino-acid transporters and Cl(-) channels.

40 cid (DIDS)-sensitive and gluconate-sensitive Cl(-) channels.

41 IP(3)R-dependent opening of Ca(2+)-activated Cl(-) channels.

42 and also whether this protein functions as a Cl- channel, a Cl-/H+ antiporter, or as something else e

43 w external Ca(2+) solution chosen to prevent Cl(-) channel activation, suggesting OMP acts upstream o

44 activation, suggesting OMP acts upstream of Cl(-) channel activation.

45 ge through the additive effects of TRPV1 and Cl- channel activation.

46 annel blocker CFTR(inh)-172 abolished apical Cl(-) channel activity in excised patches.

47 Moreover, apical Cl(-) channel activity was completely absent in principa

48 Low pH(o) activation of hClC-2 Cl(-) channel activity was PKA-dependent, retained in RG

49 Because DeltaF508-CFTR retains some Cl(-) channel activity, increased expression of DeltaF50

50 not a result of changes in cell viability or Cl(-) channel activity.

51 V mutation is associated with altered hBest1 Cl(-) channel activity.

52 tested the effect of RP-causing variants on Cl- channel activity and cellular localization of bestro

53 conductance regulator (CFTR) to inhibit its Cl- channel activity.

54 ded in this process is at least one K(+) and Cl(-) channel, allowing for both recycling of K(+) for t

55 GABA, an agonist of related Cl- channels, also triggered Cl- currents and secretion,

56 the plasma membrane and/or its function as a Cl(-) channel and conductance regulator.

57 lytopic membrane protein that functions as a Cl(-) channel and consists of two membrane spanning doma

58 s transmembrane conductance regulator (CFTR) Cl(-) channel and contribute to fluid homeostasis in the

59 m single-molecule studies of an elasmobranch Cl(-) channel and later confirmed by crystal structures

60 changes in stomatal conductance of the slac1 Cl(-) channel and ost2 H(+)-ATPase mutants, which we ver

61 The CLC protein fold is shared by Cl(-) channels and 2Cl(-):1H(+) antiporters.

62 1) and TMEM16B (ANO2), form Ca(2+)-activated Cl(-) channels and are important for transepithelial ion

63 two distinct mechanistic flavors: H(+)-gated Cl(-) channels and Cl(-)/H(+) antiporters.

64 The family of CLC proteins comprises both Cl(-) channels and Cl(-)/H(+) exchange transporters with

65 of Cl(-)-transporting proteins includes both Cl(-) channels and Cl(-)/H(+) exchange transporters.

66 The CLC protein family comprises both Cl(-) channels and H(+) -coupled anion transporters.

67 ay increase the cell surface density of CFTR Cl(-) channels and improve stability of pharmacologicall

68 channel (CLC) family comprises cell surface Cl(-) channels and intracellular Cl(-)/H(+) exchangers.

69 ngs to a family of putative Ca(2+)-activated Cl(-) channels and operates as membrane phospholipid scr

70 The TMEM16 family comprises Ca(2+)-activated Cl(-) channels and phospholipid scramblases.

71 terms of the hypotheses that bestrophins are Cl(-) channels and regulators of Ca signaling.

72 smic Cl(-) level is dynamically regulated by Cl(-) channels and transporters.

73 ipulation of epithelial ion (Na(+), K(+) and Cl(-)) channels and suppression of proinflammatory cytok

74 transduced signals through a Ca2+-activated Cl- channel and EGFR.

75 stic fibrosis transmembrane regulator (CFTR) Cl- channel and stimulation of ciliary beat frequency.

76 y phloretin, a blocker of swelling-activated Cl- channels and by flufenamic acid, a blocker of Cl- an

77 bited swelling-mediated activation of K+ and Cl- channels and cell volume recovery.

78 y, it has been proposed that bestrophins are Cl- channels and that the putative second transmembrane

79 transmembrane ion fluxes via K(+) channels, Cl(-) channels, and voltage-operated Ca(2+) channels wer

80 (ICC-IM) by activation of Ca(2+) -activated Cl(-) channels (ANO1, encoded by Ano1) and voltage-depen

81 on, the latter by opening a Ca(2+)-activated Cl channel (ANO2) to elicit, unusually, an inward Cl cur

82 Here we show that the Ca(2+)-activated Cl ((-)) channel anoctamin-1 (ANO1/TMEM16A) is located i

83 current that was effectively blocked by the Cl(-) channel antagonist 5-nitro-2-(3-phenopropylamino)b

84 relative to controls; whereas apocynin, the Cl(-) channel antagonist 5-nitro-2-(3-phenylpropylamino)

85 The GlyR Cl(-) channel antagonist strychnine significantly blocke

86 ne was blocked by pretreatment with the GlyR Cl(-) channel antagonist strychnine.

87 )-facilitated NSCC in ICC was blocked by the Cl(-) channel antagonists 4,4'-diisothiocyanatostilbene-

88 h led us to question whether functional GlyR Cl(-) channels are expressed in ASM.

89 GlyR Cl(-) channels are expressed on ASM and regulate smooth

90 response to 8-Br-cAMP, indicating that CFTR Cl(-) channels are functional in embryonic kidneys and a

91 Various K(+) and Cl(-) channels are important in cell volume regulation a

92 Because certain Cl(-) channels are proposed to promote apoptosis by redu

93 ity and surface expression of wild type CFTR Cl- channels are increased when CFTR is co-expressed wit

94 s transmembrane conductance regulator (CFTR) Cl(-) channel as a determinant in lysosomal acidificatio

95 strong possibility that the Ca(2+)-activated Cl(-) channels at the apical membrane are members of the

96 etory diarrheas increases the conductance of Cl(-) channels at the enterocyte luminal membrane, which

97 The Cl(-) channel blocker 5-nitro-2-(3-phenylpropylamino)ben

98 titution of Cl(-) ions or application of the Cl(-) channel blocker DIDS identifying it as a Ca(2+)-ac

99 flumic acid (100 microM), a Ca(2+)-activated Cl(-) channel blocker.

100 but unchanged by niflumic acid (100 mum), a Cl(-) channel blocker.

101 tro-2-(phenylpropylamino)-benzoate (NPPB), a Cl- channel blocker, reduced Isc stimulation by approxim

102 t was insensitive to apical disulphonic acid Cl(-) channel blockers, but sensitive to apical glibencl

103 well), which was reversibly inhibited by the Cl(-) channel blockers, phloretin (300 microM) or 5-nitr

104 opic taurine response was insensitive to the Cl(-) channel blockers, picrotoxin and strychnine, but i

105 )) influx that can be inhibited by selective Cl(-) channel blockers.

106 Addition of the Cl- channel blockers NPPB, glibenclamide, or bumetanide

107 The RVD was also inhibited by Cl--channel blockers and by Cl- substitution.

108 ity in a small subpopulation of F508del-CFTR Cl(-) channels but that the majority remain destabilized

109 C (100 microM) induced the openings of CFTR Cl channels by increasing its average open probability f

110 luable in the phenotypic studies of specific Cl- channels by limiting the effect of compensation on t

111 l conductance of endogenous Ca(2+)-dependent Cl- channels by lowering the energy barriers for ion tra

112 veral conductances, such as Ca(2+)-activated Cl() channels (CaCC) and non-selective cation channels (

113 Activation of an apical Ca(2+)-dependent Cl(-) channel (CaCC) is the rate-limiting step for fluid

114 The newly discovered Ca(2+)-activated Cl(-) channel (CaCC), Anoctamin 1 (Ano1 or TMEM16A), has

115 pore-forming subunit of a Ca(2+) -dependent Cl(-) channel (CaCC), is activated by direct, voltage-de

116 The Ca(2+)-activated Cl(-) channel (CaCC), recently identified as TMEM16A, pl

117 was found recently to be a calcium-activated Cl(-) channel (CaCC).

118 dent kinase II (CaMKII) and Ca(2+)-activated Cl(-) channels (CaCC) because simultaneous addition of m

119 el, and (b) secretion, by the Ca2+-activated Cl- channel (CaCC) and CFTR.

120 uctance regulator (CFTR) or a Ca2+-activated Cl- channel (CaCC).

121 An antagonist of calcium-sensitive Cl- channels (CaCC), niflumic acid, had little effect on

122 Ca(2+)-activated Cl(-) channels (CaCCs) are exceptionally well adapted to

123 Ca(2+)-activated Cl(-) channels (CaCCs) are key regulators of numerous ph

124 physiological importance of Ca(2+)-activated Cl(-) channels (CaCCs) in neurons has been largely overl

125 ily that includes TMEM16A/B Ca(2+)-activated Cl(-) channels (CaCCs) is linked to Scott syndrome with

126 t has been postulated that calcium-activated Cl(-) channels (CaCCs) play a role in airway epithelial

127 ustained by the activity of Ca(2+)-activated Cl(-) channels (CaCCs).

128 ctance regulator (CFTR) and Ca(2+)-activated Cl(-) channels (CaCCs).

129 n may occur via activation of Ca2+-activated Cl- channels (CaCCs) or an increase in the Cl- driving f

130 Ca(2+)-activated Cl- channels (CaCCs) perform many important functions in

131 have deleterious mutations in an epithelial Cl(-) channel called the CF transmembrane conductance re

132 channel in turn activates a Ca(2+)-activated Cl(-) channel, causing a Cl(-) efflux and further depola

133 s transmembrane conductance regulator (CFTR) Cl(-) channel, causing airway surface liquid dehydration

134 fibrosis transmembrane conductance regulator Cl- channel (CFTR) participates in phagosomal pH control

135 Although commonly known as a Cl(-) channel, CFTR also conducts thiocyanate (SCN(-)) i

136 K(+) channel Kir4.1, and stimulation of the Cl(-) channel ClC-K.

137 The voltage-gated Cl(-) channel (CLC) family comprises cell surface Cl(-)

138 The Ca2+-activated Cl- channel (CLCA) inhibitor, niflumic acid (NFA, 100 mi

139 here we demonstrate that the C. elegans ClC Cl(-) channel CLH-1 is highly permeable to HCO3 (-) and

140 on was initiated by Cl - secretion via ClC-2 Cl - channels co-expressed with occludin and localized t

141 cal component of the acinar Ca(2+)-activated Cl(-) channel complex that is essential for saliva produ

142 to insulin is mediated through exocytosis of Cl- channel-containing vesicles and a subsequent opening

143 pore region of the TMEM16A Ca(2+)-activated Cl(-) channel convert it into a robust scramblase.

144 nward-rectifying K+ channels and background (Cl- channel) current, and to a parallel loss in sensitiv

145 The cAMP-activated Cl(-) channel cystic fibrosis transmembrane conductance

146 ful approach to understanding the epithelial Cl(-) channel cystic fibrosis transmembrane conductance

147 conductance regulator (CFTR) is an ATP-gated Cl(-) channel defective in the genetic disease cystic fi

148 linity, we used mutants of the only vacuolar Cl(-) channel described to date: the Arabidopsis (Arabid

149 ast, picrotoxin, which blocks the GABA-gated Cl- channel, did not inhibit the secondary rise in [Cl-]

150 transmembrane conductance regulator (CFTR, a Cl(-) channel) disrupt salt and fluid transport and lead

151 eutral ion channel, and of GlyR, an inactive Cl(-) channel, do not cause CFAs, demonstrating that cor

152 the first observation of the involvement of Cl(-) channels during the HCV life cycle.

153 -) ion channels, it is controversial whether Cl(-) channel dysfunction can explain the diseases.

154 (ICC-IM) by activation of Ca(2+) -activated Cl(-) channels (encoded by Ano1) and voltage-dependent L

155 Previously, we provided evidence that single Cl-channel events underlie DAT-1 currents.

156 3',5'-cyclic monophosphate (cAMP)-stimulated Cl(-) channel expressed in cholangiocytes.

157 uctance regulator (CFTR) is a cAMP-activated Cl(-) channel expressed in the apical membrane of fluid-

158 e regulator (CFTR) is a cyclic AMP-regulated Cl(-) channel expressed in the apical plasma membrane in

159 uctance regulator (CFTR) is a cAMP-activated Cl(-) channel expressed in the apical plasma membrane of

160 brane conductance regulator (CFTR) chloride (Cl(-)) channel expression and fluid secretion in the air

161 The CLC 'Cl(-) channel' family consists of both Cl(-)/H(+) antipo

162 om two distinct families of Ca(2+)-activated Cl(-) channels found in salivary glands.

163 lation of the function of ClC-0, a chloride (Cl(-)) channel from the Torpedo electric organ.

164 Regulation of the CFTR Cl channel function involves a protein complex of activa

165 Q1291F CFTR displayed significantly reduced Cl(-) channel function in well differentiated primary hu

166 ns of adenosine 5'-monophosphate (AMP), CFTR Cl(-) channel function is coupled to adenylate kinase ac

167 rmine whether the A243V mutation affects the Cl(-) channel function of hBest1.

168 rophy (BVMD) is caused by dysfunction in the Cl(-) channel function of human bestrophin-1 (hBest1), b

169 re reported to alter Na(+), K(+), Ca(2+) and Cl(-) channel function, intracellular [Ca(2+)], and Na(+

170 A243V mutations does not correlate with the Cl(-) channel function, the results also support the sug

171 26a9 has both nCl(-)-HCO(3)(-) exchanger and Cl(-) channel function.

172 the effect of the hBest1 mutation on hBest1 Cl(-) channel function.

173 except L567F and T216I produced a defect in Cl(-) channel function.

174 suggesting that this mutation may not affect Cl(-) channel function.

175 erated AFC in this model is due to increased Cl- channel function.

176 a Ca(2+) influx that opens Ca(2+)-activated Cl(-) channels, generating the receptor potential.

177 nt studies have identified several chloride (Cl-) channel genes in the heart, including CFTR, ClC-2,

178 A modified invertebrate glutamate-gated Cl(-) channel (GluCl alphabeta) was previously employed

179 lumic acid, an inhibitor of Ca(2+)-activated Cl(-) channels, had no effect.

180 cently a novel cGMP-activated Ca2+-dependent Cl- channel has been described in rat mesenteric artery

181 e large superfamily of ClC voltage-dependent Cl(-) channels, has been proposed as a molecular candida

182 Until recently, anion (Cl(-)) channels have received considerably less attentio

183 iously prime candidates for Ca(2+)-activated Cl(-) channels, have been supplanted by the newly discov

184 or pathophysiological phenotypes of cardiac Cl- channels, however, may be complicated by the compens

185 functions as a Cl(-)/H(+) antiporter, not a Cl(-) channel; however, the molecular mechanism for Cl(-

186 fibrosis transmembrane conductance regulator Cl(-) channel; however, the relative alignment of these

187 with their inhibition of swelling-activated Cl(-) channels (I(Clvol)), suggesting that I(Clvol) medi

188 stigated the contributory role of individual Cl - channels in the recovery of barrier function in isc

189 ibrosis transmembrane conductance regulator, Cl(-) channel in BECs and suggest that TMEM16A may be a

190 n apical cell membranes or its function as a Cl(-) channel in native renal epithelia has not been dem

191 s of a novel cGMP-activated Ca(2+)-dependent Cl(-) channel in rat mesenteric artery smooth muscle cel

192 ods, Eriksen et al. (2016) have identified a Cl(-) channel in the transporter that is coactivated by

193 tically subjective essay recalls the Torpedo Cl(-) channel in the years when it had neither a molecul

194 experiments revealed expression of GABA(A)R Cl(-) channels in 52% of beta-cells (current density 9 p

195 nm) and suppressed opening of cAMP-dependent Cl(-) channels in cardiac myocytes (IC(50) approximately

196 s transmembrane conductance regulator (CFTR) Cl(-) channels in mammalian cells revealed confined diff

197 compelling evidence that activation of CFTR Cl(-) channels in mouse heart are coupled to G-protein c

198 Cl(-) channels in the apical membrane of biliary epithel

199 CFTR forms protein kinase A (PKA)-activated Cl(-) channels in the apical membrane of principal cells

200 the local apical Ca2+ spikes that switch on Cl(-) channels in the apical plasma membrane as well as

201 c reticulum and leads to the absence of CFTR Cl(-) channels in the apical plasma membrane.

202 We summarise what is known regarding Cl(-) channels in the ER/SR and the non-selective cation

203 d, in part, by modulating the number of CFTR Cl(-) channels in the plasma membrane by adjusting CFTR

204 TMEM16A), also termed Anoctamin 1, chloride (Cl(-)) channels in arterial myocytes.

205 solute carrier family 26, member 9 (SLC26A9) Cl- channel in asthma, we induced Th2-mediated inflammat

206 g of the integrated function of each cardiac Cl- channel in the context of health and disease.

207 m [Ca2+]i with 1 microm CaM did not activate Cl- channels in the absence of cGMP.

208 to delineate the functional role of cardiac Cl- channels in the context of health and disease.

209 We summarise what is known regarding Cl- channels in the ER/SR and the non-selective cation c

210 ted (CNG) channel, leading to Ca2+ gating of Cl- channels; in TRPM5-GFP+ OSNs, the Ca2+ -activated Cl

211 mulates cAMP production to activate the CFTR Cl(-) channel, increase ciliary beating, and initiate cy

212 Natural-product diarrhea remedies with Cl(-) channel inhibition activity have also been identif

213 apid, protein kinase C (PKC)-dependent ClC-1 Cl(-) channel inhibition in rodent muscle.

214 RNA)-mediated silencing, we demonstrate that Cl(-) channel inhibition is detrimental to HCV replicati

215 Exposure to a Cl(-) channel inhibitor 5-nitro-2-(3-phenylpropylamino)b

216 ree" solution and blocked by the nonspecific Cl(-) channel inhibitor niflumic acid and by preincubati

217 trans-membrane conductance regulator (CFTR) Cl(-) channel is a multimer.

218 Bestrophin-2 (Best2), a putative Cl(-) channel is expressed in the nonpigmented epitheliu

219 molecular identity of this Ca(2+)-activated Cl(-) channel is unknown.

220 Although activation of outward rectifying Cl(-) channels is one of the fastest responses of endoth

221 Our data demonstrate that the SLC26A9 Cl- channel is activated in airway inflammation and sugg

222 Knowledge of how ATP gates the CFTR Cl- channel is critical for understanding CFTR's physiol

223 It is not known whether the activity of Cl- channels is altered in insulin resistance and by whi

224 that electrolyte and fluid efflux via K+ and Cl- channels is controlled by swelling-induced activatio

225 Ano1 (Tmem16a), a Ca(2+)-activated Cl(-) channel, is an ion channel expressed in ICC.

226 amongst other factors, the expression of the Cl channel kidney-specific chloride channel 1 and its su

227 ClC Cl- channels make up a large molecular family, ubiquitou

228 s transmembrane conductance regulator (CFTR) Cl(-) channel may be of value in developing new treatmen

229 ructurally unrelated prosecretory intestinal Cl(-) channels may account for its intestinal antisecret

230 It has been shown that Cl- channels may contribute to cardiac arrhythmogenesis,

231 The integrated function of Cl- channels may involve multi-protein complexes of the

232 CFTR Cl- channels may serve as novel and crucial mediators in

233 ermined in the intestine, this voltage-gated Cl(-) channel might compensate for the secretory defects

234 16A) and ANO2 (TMEM16B) are Ca(2+)-activated Cl(-) channels, most ANO paralogs are Ca(2+)-dependent p

235 s transmembrane conductance regulator (CFTR) Cl(-) channel mutations cause cystic fibrosis lung disea

236 y reflect upregulation of swelling-activated Cl(-) channels of different subtypes, especially when th

237 sed by defects in the CFTR, a cAMP-activated Cl- channel of epithelia.

238 regulates inward-rectifying K+ channels and Cl- channels of Vicia guard cells via intracellular Ca2+

239 aying, in part via the LGC-55 tyramine-gated Cl(-) channel on the HSNs.

240 ss the physiologic implications of open CFTR Cl(-) channels on salt handling by the collecting duct a

241 ation by Na(+)-coupled uptake, glycine opens Cl(-) channels on the surface membrane.

242 ed the effects of fatty acid accumulation on Cl- channel opening in a model liver cell line.

243 ion of PKC partially restored exocytosis and Cl- channel opening in insulin-resistant cells.

244 r, insulin failed to activate exocytosis and Cl- channel opening.

245 sporters form dimers that function either as Cl(-) channels or as electrogenic Cl(-)/H(+) exchangers.

246 The maxi Cl- channel (p-VDAC) blocker Gd3+, the ClC-2 inhibitor C

247 e that hClCa1 does not form Ca(2+)-dependent Cl- channels per se or enhance the trafficking/insertion

248 One reason for this may be that many Cl(-) channels perform functions that might be considere

249 ad no effect, suggesting that flow-activated Cl(-) channels play an important role in regulating EC f

250 s transmembrane conductance regulator (CFTR) Cl- channel plays vital roles in fluid transport in many

251 ator (CFTR), in addition to its well defined Cl- channel properties, regulates other ion channels.

252 ine CFTR formed a weakly inwardly rectifying Cl(-) channel regulated by PKA-dependent phosphorylation

253 Enterocyte Cl(-) channels represent an attractive class of targets

254 fibrosis transmembrane conductance regulator Cl(-) channel requires a functionally unique, positively

255 the plasma membrane, and it blocked K(+) and Cl(-) channel responses to abscisic acid in guard cells.

256 is thought to function as a Ca(2+)-activated Cl(-) channel, RPE cells from Best1(W93C) mice exhibited

257 We set out to identify Cl(-) channel(s) and/or transporter(s) that are regulate

258 channels (VDCCs) or TMEM16A Ca(2+)-activated Cl(-) channels significantly changes global cytosolic Ca

259 s may involve multi-protein complexes of the Cl- channel subproteome and similar phenotypes can be at

260 Our results identify the first Cl(-) channel target of the CLCA family of proteins and

261 Bestrophin is thought to be the Cl channel that generates the LP.

262 nductance regulator (CFTR), a cAMP-dependent Cl channel that regulates epithelial surface fluid secre

263 ligand-gated ion channels, is an inhibitory Cl(-) channel that is gated by glycine.

264 gs reveal that SLC26A7 functions as a unique Cl(-) channel that is regulated by intracellular H(+).

265 rst described as a family of plasma membrane Cl(-) channels that could be activated by calcium.

266 The cftr gene codes for a Cl(-) channel, the cystic fibrosis transmembrane conduct

267 Chloride influx through GABA-gated Cl(-) channels, the principal mechanism for inhibiting n

268 ace in mice through Ca2+- and cAMP-sensitive Cl- channels, the latter pathway being the cystic fibros

269 quence of an activation of [Ca2+]c sensitive Cl- channels, the model simulations compare well with th

270 mediated by activation of Ca(2+) -activated Cl(-) channels; thus, Ca(2+) signalling is central to th

271 gly inhibit the intestinal calcium-activated Cl(-) channel TMEM16A by a voltage-independent inhibitio

272 d the protein levels of the Ca(2+)-activated Cl(-) channel TMEM16A, the major apical Cl(-) efflux pat

273 family, which includes the Ca(2+)-activated Cl(-) channels TMEM16A and TMEM16B and a small-conductan

274 hy with subcortical cysts, targets the CLC-2 Cl(-) channel to cell contacts in glia and activates CLC

275 rks can additionally activate Ca2+-activated Cl(-) channels to generate spontaneous transient inward

276 CaMKII) activation of ClC-3, a voltage-gated Cl(-) channel/transporter, because pharmacological inhib

277 validated the idea that ions permeate TMEM16 Cl(-) channels via a structurally homologous pathway by

278 tructural components of the volume-regulated Cl(-) channel (VRAC), and we underline the intriguing po

279 ial of the inward current, indicating that a Cl- channel was not involved.

280 The expression of candidate Cl- channels was confirmed by RT-PCR.

281 n agonist of glycine receptor chloride (GlyR Cl(-)) channels, was found to relax contracted ASM, whic

282 To study individual CFTR Cl(-) channels, we performed single-channel recording, w

283 Ca2+ -activated Cl channels were recently discovered to be encoded by me

284 These Cl(-) channels were observed in cell-attached apical pat

285 Quiescent Cl(-) channels were present in patches excised from untr

286 ce, kinetics, and anion selectivity of these Cl(-) channels were the same as those of recombinant mou

287 elopment of agents that act directly to open Cl channels, which thereby increases the liquidity of th

288 stic fibrosis transmembrane regulator (CFTR) Cl(-) channel, which is regulated by phosphorylation in

289 trimerization domains is a partially formed Cl(-) channel, which opens to form a pore through which

290 e Ca(2+) activates Ca(2+)-dependent K(+) and Cl(-) channels, which participate in bleb regulation.

291 conductance regulator (CFTR) is a chloride (Cl(-)) channel, which plays an important role in physiol

292 ters, especially potassium (K) and chloride (Cl) channels, which secondarily affect function of the N

293 Single Ca(2+)-activated Cl() channels with a unitary conductance of 7.8 pS were

294 e conclude that ovine CFTR forms a regulated Cl(-) channel with enhanced conductance and ATP-dependen

295 stic fibrosis transmembrane regulator (CFTR) Cl(-) channel with maximum inhibition of approximately 6

296 we report that SLC26A9 is a highly selective Cl(-) channel with minimal OH(-)/HCO(3)(-) permeability

297 These findings indicate that SLC26A9 is a Cl(-) channel with minimal OH(-)/HCO(3)(-) permeability.

298 cells SLC26A7 functions as a pH(i)-regulated Cl(-) channel with minimal OH(-)/HCO(3)(-) permeability.

299 discuss the recent explosion of interest in Cl(-) channels, with special emphasis on new and often s

300 amins and now hold a tenuous position in the Cl(-) channel world.